Subacute myelo-optic neuropathy and clioquinol. An epidemiological case-history for diagnosis.

Meade, Tanya

doi:10.1136/jech.29.3.157

Cited by 43 publications

(41 citation statements)

References 19 publications

(20 reference statements)

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“…1A), a lipophilic compound capable of forming stable complexes with copper(II) ions (25), was used as an antibiotic for treating diarrhea and skin infection (26). Although clioquinol use was thought to be associated with occurrence of subacute myelo-optic neuropathy in Japan (25)(26)(27), this conclusion was not supported by the subsequent epidemiologic analysis (28). Instead, decreased levels of vitamin B 12 may play a role in this syndrome (26).…”

Section: Introductioncontrasting

confidence: 38%

Clioquinol, a Therapeutic Agent for Alzheimer's Disease, Has Proteasome-Inhibitory, Androgen Receptor–Suppressing, Apoptosis-Inducing, and Antitumor Activities in Human Prostate Cancer Cells and Xenografts

et al. 2007

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Section: Introductioncontrasting

confidence: 38%

Clioquinol, a Therapeutic Agent for Alzheimer's Disease, Has Proteasome-Inhibitory, Androgen Receptor–Suppressing, Apoptosis-Inducing, and Antitumor Activities in Human Prostate Cancer Cells and Xenografts

et al. 2007

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“…This report included 4000 individuals and over a 4-year period, and showed few side effects [89]. Although CQ use was thought to be associated with the occurrence of subacute myelo-optic neuropathy in Japan [90][91][92], this conclusion was not supported by the subsequent epidemiologic analysis [93]. Instead, decreased levels of vitamin B 12 may play a role in this syndrome [92].…”

Section: Drugs In Hydroxyquinoline Familymentioning

confidence: 45%

New uses for old copper-binding drugs: converting the pro-angiogenic copper to a specific cancer cell death inducer

Chen

Dou

2008

Expert Opinion on Therapeutic Targets

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Background-The conventional approach toward anticancer drug development is a timeconsuming and expensive procedure.Objective/methods-One approach to expedite this process and achieve more affordable means is to discover new applications of existing drugs, since their pharmacokinetics and pharmacological profiles are well known.Results-Our encouraging findings in recent studies reveal anticancer activities of several copper-binding ligands including disulfiram (an antialcoholism drug), clioquinol (used to treat Alzheimer's and Huntington's diseases) and diethyldithiocarbamate (an agent for HIV-1 infection treatment). Conclusion-These in vitro and in vivo studies have demonstrated that these archaic drugs cantarget and react with tumor cellular copper, forming complexes that act as potent proteasome inhibitors and apoptosis inducers.

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“…In fact, intramuscular administration of the prototype iron chelator desferrioxamine (DFO) slowed the clinical progression of AD dementia [97] , and some success has also been achieved with another metal-complexing agent, clioquinol [98] . However, clioquinol is highly toxic [99] and DFO has poor penetration across the blood-brain barrier [17] . Fig.…”

Section: Metal-chelating Activitymentioning

confidence: 99%

Multifunctional Activities of Green Tea Catechins in Neuroprotection

Mandel¹,

Avramovich-Tirosh²,

Reznichenko³

et al. 2005

Neurosignals

310

111

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Many lines of evidence suggest that oxidative stress resulting in reactive oxygen species (ROS) generation and inflammation play a pivotal role in the age-associated cognitive decline and neuronal loss in neurodegenerative diseases including Alzheimer’s (AD), Parkinson’s (PD) and Huntington’s diseases. One cardinal chemical pathology observed in these disorders is the accumulation of iron at sites where the neurons die. The buildup of an iron gradient in conjunction with ROS (superoxide, hydroxyl radical and nitric oxide) are thought to constitute a major trigger in neuronal toxicity and demise in all these diseases. Thus, promising future treatment of neurodegenerative diseases and aging depends on availability of effective brain permeable, iron-chelatable/radical scavenger neuroprotective drugs that would prevent the progression of neurodegeneration. Tea flavonoids (catechins) have been reported to possess potent iron- chelating, radical-scavenging and anti-inflammatory activities and to protect neuronal death in a wide array of cellular and animal models of neurological diseases. Recent studies have indicated that in addition to the known antioxidant activity of catechins, other mechanisms such as modulation of signal transduction pathways, cell survival/death genes and mitochondrial function, contribute significantly to the induction of cell viability. This review will focus on the multifunctional properties of green tea and its major component (–)-epigallocatechin-3-gallate (EGCG) and their ability to induce neuroprotection and neurorescue in vitro and in vivo. In particular, their transitional metal (iron and copper) chelating property and inhibition of oxidative stress.

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Subacute myelo-optic neuropathy and clioquinol. An epidemiological case-history for diagnosis.

Cited by 43 publications

References 19 publications

Clioquinol, a Therapeutic Agent for Alzheimer's Disease, Has Proteasome-Inhibitory, Androgen Receptor–Suppressing, Apoptosis-Inducing, and Antitumor Activities in Human Prostate Cancer Cells and Xenografts

Clioquinol, a Therapeutic Agent for Alzheimer's Disease, Has Proteasome-Inhibitory, Androgen Receptor–Suppressing, Apoptosis-Inducing, and Antitumor Activities in Human Prostate Cancer Cells and Xenografts

New uses for old copper-binding drugs: converting the pro-angiogenic copper to a specific cancer cell death inducer

Multifunctional Activities of Green Tea Catechins in Neuroprotection

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